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Case Report

Tuberculous Peritonitis Mimicking Ovarian Cancer

Javier E. Fajardo, MD; In³s M. Gonzàlez, MD; Yvonne Collins, MD; Dietrich Werner, MD; Jean Hurteau, MD

Tuberculous peritonitis is a rare condition that might be confounded with ovarian cancer. The combination of vague gastrointestinal symptoms, ascites, and elevated levels of cancer anti- gen 125 (CA 125) suggests ovarian malignancy, but benign conditions should be considered as well.

Extrapulmonary tuberculosis may mimic various malignant conditions. The literature reflects the challenge to the gynecologist in establishing the diagnosis of pelvic tuberculosis, which is often confused with ovarian cancer.1,2 Specifically, both pelvic tuberculosis and ovarian cancer share vague symptoms (eg, abdominal pain and fullness/pressure, anorexia, weight loss, ascites), plus elevations in CA 125 levels. While still considered an uncommon disease, the number of peritoneal tuberculosis cases has risen in recent years due to the influx of immigrants from countries with a higher prevalence of tuberculosis.3 Although the incidence of tuberculosis is greater in patients with human immunodeficiency virus or acquired immunodeficiency syndrome, this population does not have an increased frequency of tuberculous peritonitis.4 The condition is also more common among patients with alcohol-related liver disease—especially those from Western countries. Indeed, it is estimated that 60% of patients with tuberculous peritonitis have underlying alcoholic liver disease, compared with 10% in patients from developing countries.5

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CASE REPORT

A 32-year-old Hispanic woman (gravida 3, para 3) was referred secondary to a 3-month history of abdominopelvic pain aggravated by activity. Other symptoms included bloating, early satiety, and an 11-lb weight loss over the last 3 months despite unchanged appetite. The patient's medical history was significant for gastroesophageal reflux disease treated with famotidine. Her surgical history included one cesarean delivery. The patient’s family history was significant for a maternal grandmother with uterine cancer, father’s second cousin with breast cancer, and maternal uncle with throat cancer. Physical findings were otherwise unremarkable, with no tenderness or masses palpable either abdominally or vaginally.

Laboratory findings included a normal complete blood cell count and an elevated serum CA 125 level at 99 U/mL. Transvaginal ultrasonography revealed small cysts on both ovaries but no enlargement, with free fluid in the cul-de-sac. Computed tomography (CT) showed clear lung bases; a cystic lesion within the liver with potential thickening of the undersurface of the diaphragm; possible mesenteric and omental stranding; enlarged, low-density lymph nodes in the porta hepatis; and ascites. Based on these findings, the patient was scheduled for initial diagnostic laparoscopy followed by possible exploratory laparotomy for staging if indicated.

Entry was achieved via an open technique. A gross survey revealed a moderate amount of ascites, with multiple excrescences on the peritoneal and serosal intestinal surfaces—as well as all other surfaces in the abdominopelvic cavity (including the liver and falciform ligament). No gross masses were noted. The ovaries could not be visualized, as the cul-de-sac was obliterated by adhesions. Peritoneal fluid was sent for cytology, and numerous biopsy samples were taken. Frozen sections of the specimens from different areas were consistent with inflammatory pseudotumor.

Cytology of the peritoneal fluid was negative for malignancy. Lymphocytes and mesothelial cells were present, some with reactive changes and macrophages. The final histologic analysis suggested granulomatous inflammation with necrosis and proliferation of reactive fibroblasts, as well as central necrosis with areas of caseation (Figure). An acid-fast bacilli culture of the peritoneal nodules yielded Mycobacterium tuberculosis complex.

Antituberculosis treatment was initiated, and the patient reported improvement of symptoms 6 weeks later. Further follow-up was not possible, as the patient returned to her native country without notification.

Figure not available online

Figure. Tuberculoid granulomas with central caseous necrosis (hematoxylin and eosin X 200). Courtesy of Javier E. Fajardo, MD.

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DISCUSSION

Mycobacterium tuberculosis infects 32% of the global population, accounting for 8 million new cases of tuberculosis and approximately 2 million deaths annually worldwide.6 Tuberculous peritonitis occurs in 0.1% to 0.7% of all cases of tuberculosis,7 and can be divided clinically into plastic and serous types. Tender abdominal masses and a “doughy abdomen” characterize the less common plastic type. The serous type presents classically with fever, chronic abdominal pain, weight loss, and ascites—ie, the symptoms occurring in the patient featured here (except for fever).

The combination of these symptoms with the presence of ascites in imaging studies plus elevated serum CA 125 values suggested the possibility of ovarian cancer. Levels of CA 125 are increased in various benign gynecologic and nongynecologic conditions, including tuberculous peritonitis. Most of the case series reported come from Germany and Turkey. In 2004, 11 cases were reported in Turkey: nine with peritoneal tuberculosis and two with colonic tuberculosis. Seven of the patients were women, four of whom had elevated CA 125 levels (all with peritoneal tuberculosis).8

Some benign gynecologic conditions that may inflame the peritoneum (eg, endometriosis, pelvic inflammatory disease, ovarian hyperstimulation syndrome) can cause CA 125 elevations due to chronic inflammation of mesothelial cells on the peritoneal surface. It has been suggested that in many diseases characterized by the presence of ascites (eg, Meigs syndrome, tuberculous peritonitis), CA 125 might be synthesized by the peritoneal epithelium as a response to a mechanical insult, subsequently passing from the peritoneal cavity to the serum through the peritoneum.

In patients with tuberculous peritonitis, the peritoneal fluid is exudative, usually containing 500 to 2,000 cells/mL. Lymphocytes typically predominate, although in some cases polymorphonuclear leukocytes are more abundant early in the process. Measurement of adenosine deaminase activity in ascitic fluid appears to have a high degree of sensitivity (86%) and specificity (100%).9 Therefore, ultrasonography or CT-guided paracentesis may be considered as a diagnostic tool in patients with suspected tuberculous peritonitis. In patients for whom the suspicion of ovarian cancer is unclear and other diagnoses are possible based on the presence of vague symptoms, ascites, and elevated CA 125 values, diagnostic laparoscopy can also be a valuable approach, with lower costs and morbidity compared with exploratory laparotomy.

The treatment for tuberculous peritonitis is the same as for pul- monary tuberculosis. The bene-ficial effects of adjunctive corticosteroid therapy have not been established definitively, although the available data suggest a modest benefit including a decreased risk of late intestinal obstruction and adhesion formation.10

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CONCLUSION

Tuberculous peritonitis can be confused with multiple diseases. Given the influx of immigrants from at-risk areas of the world, it now merits routine consideration in the differential diagnosis—particularly when ovarian cancer is suspected. If tuberculous peritonitis is suspected, then laparoscopy is the preferred avenue of approach.

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Javier E. Fajardo, MD, is resident, Department of Obstetrics and Gynecology. Yvonne Collins, MD, is assistant professor, Division of Gynecologic Oncology, Department of Obstetrics and Gynecology. Jean Hurteau, MD, is professor and director, Division of Gynecologic Oncology, Department of Obstetrics and Gynecology. Dietrich Werner, MD, is surgical pathology fellow, Department of Pathology. All are at the University of Illinois Medical Center, Chicago. In³s M. Gonzàlez, MD, is infectious disease fellow, Department of Internal Medicine, Rush University Medical Center, Chicago, Ill.

References

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2. Protopapas A, Milingos S, Diakomanolis E, et al. Miliary tuberculous peritonitis mimicking advanced ovarian cancer. Gynecol Obstet Invest. 2003;56(2):89-92.
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5. Shakil AO, Korula J, Kanel GC, Murray NG, Reynolds TB. Diagnostic features of tuberculous peritonitis in the absence and presence of chronic liver disease: a case control study. Am J Med. 1996;100(2):179-185.
6. Dye C, Scheele S, Dolin P, Pathania V, Raviglione MC. Consensus statement. Global burden of tuberculosis: estimated incidence, prevalence, and mortality by country. WHO Global Surveillance and Monitoring Project. JAMA. 1999;282(7):677-686.
7. Vyravanathan S, Jeyarajah R. Tuber- culous peritonitis: a review of thirty-five cases. Postgrad Med J. 1980;56(659):649-651.
8. Uzunkoy A, Harma M, Harma M. Diagnosis of abdominal tuberculosis: experience from 11 cases and review of the literature. World J Gastroenterol. 2004;10(24):3647-3649.
9. Fernandez-Rodriguez CM, Perez-Arguelles BS, Ledo L, Garcia-Vila LM, Pereira S, Rodriguez-Martinez D. Ascites adenosine deaminase activity is decreased in tuberculous ascites with low protein content. Am J Gastroenterol. 1991;86(10):1500-1503.
10. Haas DW. Is adjunctive corticosteroid therapy indicated during tuberculous peritonitis? Clin Infect Dis. 1998;27(1):57-58.

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